Interleukin-33 (IL-33) as a Diagnostic and Prognostic Factor in Traumatic Brain Injury

Interleukin-33 (IL-33) is a cytokine involved in interleukin-1 family. Role of IL-33 in immune system activation is well described in the literature. IL-33 has been identified as an endogenous alarm signal (alarmin) to alert various types of immune cells to trauma. In this narrative review, we aimed to underline the diagnostic and prognostic importance of IL-33 in trauma, particularly in brain trauma.

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Abstract P145: Renal Inflammation and Injury is Associated with Increased Lymphangiogenesis in Hypertension

Hypertension ◽

10.1161/hyp.68.suppl_1.p145 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Sterling C Kneedler ◽

Lauren Phillips ◽

Kayla R Hudson ◽

Katharine M Beckman ◽

Alan R Parrish ◽

...

Keyword(s):

Blood Pressure ◽

Immune System ◽

Immune Cells ◽

Lymphatic Vessels ◽

Macrophage Infiltration ◽

Shr Rats ◽

Renal Inflammation ◽

Immune System Activation ◽

System Activation ◽

Fischer Rats

Hypertension is associated with immune system activation and inflammation. Renal infiltration of both innate and adaptive immune cells contributes to injury, dysfunction, and increased blood pressure. Activated immune cells that exit blood vessels into the interstitium then travel through lymphatic vessels to draining lymph nodes where they signal to other immune cells to increase the immune response. It is unknown how renal lymphatic vessels change in the context of hypertension, immune system activation, inflammation, and injury. We hypothesized that renal macrophage infiltration, inflammation, and injury would significantly increase lymphangiogenesis in various strains of rats. SHR rats that exhibit hypertension and renal injury (SHR-A3 strain) had significantly increased numbers of renal lymphatic vessels at 40 weeks of age compared to WKY controls (total of 3 fields of view: 52 ± 1 vs. 28 ± 1; p<0.05). This was associated with increased renal macrophage infiltration. SHR rats that exhibit hypertension but minimal renal injury (SHR-B2 strain) had significantly less renal lymphatic vessel numbers compared to WKY controls (25 ± 2 vs. 28 ± 1; p<0.05) and normal levels of macrophages. The signals for lymphangiogenesis, VEGF-C and its receptor VEGF-R3, were both increased significantly at the protein level in the kidneys of SHR-A3 rats at 18 weeks but not different in the kidneys of SHR-B2 rats compared to WKY controls. To test whether the increased lymphangiogensis is due to hypertension and/or renal inflammation and injury, we obtained kidneys from Fischer 344 rats that exhibit normal blood pressure but develop renal inflammation and injury as they age. Compared to kidneys from control 4-month old Fischer rats, kidneys from 20-month and 24-month old Fischer rats had significantly increased numbers of lymphatic vessels (32 ± 3 vs. 74 ± 1 vs. 110 ± 6, respectively; p<0.05) and this was also associated with increased macrophage infiltration. Protein levels of VEGF-C and VEGF-R3 were increased significantly in 20-month old Fischer rats compared to 4-month old controls. These data together demonstrate that renal immune cell infiltration, inflammation, and injury increases lymphangiogenesis.

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Immune system activation and fatigue during treadmill running: role of interferon

Medicine & Science in Sports & Exercise ◽

10.1097/00005768-199806000-00014 ◽

1998 ◽

Vol 30 (6) ◽

pp. 863-868 ◽

Cited By ~ 11

Author(s):

J. M. DAVIS ◽

J. A. WEAVER ◽

M. L. KOHUT ◽

L. H. COLBERT ◽

A. GHAFFAR ◽

...

Keyword(s):

Immune System ◽

Treadmill Running ◽

Immune System Activation ◽

System Activation

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Perspectives on the Role of Photodynamic Therapy in the Treatment of Pancreatic Cancer

International Journal of Photoenergy ◽

10.1155/2012/637429 ◽

2012 ◽

Vol 2012 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Wei Li ◽

Qingyong Ma ◽

Erxi Wu

Keyword(s):

Pancreatic Cancer ◽

Photodynamic Therapy ◽

Experimental Studies ◽

Oxygen Species ◽

Tumor Cell Death ◽

Antitumor Effects ◽

Immune System Activation ◽

System Activation ◽

Photosensitizing Agent

Photodynamic therapy (PDT) is a noninvasive procedure involving a photosensitizing agent that is activated by light to produce reactive oxygen species (ROS) that selectively destroy tumor cells. In recent years, PDT has been used in the treatment of pancreatic cancer (PC). The antitumor effects of PDT include three main mechanisms: direct tumor cell death (necrosis, apoptosis, and autophagy), vascular destruction, and immune system activation. The present paper systematically summarizes the effects of PDT in the treatment of PC from the experimental studies to the clinical studies and discusses the mechanisms of PDT-induced PC destruction.

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Role of IL-33 and Its Receptor in T Cell-Mediated Autoimmune Diseases

BioMed Research International ◽

10.1155/2014/587376 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 13

Author(s):

Qing Zhao ◽

Guangjie Chen

Keyword(s):

T Cell ◽

Autoimmune Diseases ◽

Host Defense ◽

Interleukin 1 ◽

Target Cells ◽

Specific Receptor ◽

Interleukin 33 ◽

New Findings ◽

Organ Specific

Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.

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The Contradictory Role of Interleukin-33 in Immune Cells and Tumor Immunity

Cancer Management and Research ◽

10.2147/cmar.s262745 ◽

2020 ◽

Vol Volume 12 ◽

pp. 7527-7537

Author(s):

Xujun Zhang ◽

Wenbiao Chen ◽

Ping Zeng ◽

Jia Xu ◽

Hongyan Diao

Keyword(s):

Tumor Immunity ◽

Immune Cells ◽

Interleukin 33

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Comparisons of lung and gluteus transcriptome profiles between yaks at different ages

Scientific Reports ◽

10.1038/s41598-019-50618-x ◽

2019 ◽

Vol 9 (1) ◽

Author(s):

Jin-Wei Xin ◽

Zhi-Xin Chai ◽

Cheng-Fu Zhang ◽

Qiang Zhang ◽

Yong Zhu ◽

...

Keyword(s):

Immune System ◽

Immune Function ◽

Muscle Injury ◽

Tibet Plateau ◽

Immune Functions ◽

Immune System Activation ◽

System Activation ◽

Qinghai Tibet Plateau ◽

Activation Status

Abstract The yak, Bos grunniens, is the only large mammal in the Qinghai-Tibet Plateau and has been bred to provide meat, milk, and transportation. Previous studies indicate that the immune system contributes to the yak’s adaptation to high-altitude environments. In order to further investigate changes in immune function during yak development, we compared the transcriptome profiles of gluteus and lung tissues among yaks at 6, 30, 60, and 90 months of age. Analyses of significantly differentially expressed genes (DEGs) in lung tissues revealed that immune function was more activated at 6-months and less activated at 90-months than in the 30 and 60-month-old animals. DEG exploration in gluteal tissues revealed that immune functions were more highly activated at both 6 and 90-months, compared with 30 and 60-months. Immune system activation in the muscle and lung tissues of 30-month-old yaks may increase their resistance to infections, while decreased may be due to aging. Furthermore, the higher immune activation status in the gluteal tissues in 90-month-old yaks could be due to muscle injury and subsequent regeneration, which is supported by the fact that 5 unigenes related with muscle injury and 3 related to muscle regeneration displayed greater expression levels at 90-months than at 30 and 60-months. Overall, the present study highlights the important role of the immune system in yak development, which will facilitate future investigations.

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Inflammation and Immune System Activation After Traumatic Brain Injury

Current Neurology and Neuroscience Reports ◽

10.1007/s11910-014-0484-2 ◽

2014 ◽

Vol 14 (10) ◽

Cited By ~ 21

Author(s):

Ramani Balu

Keyword(s):

Traumatic Brain Injury ◽

Immune System ◽

Brain Injury ◽

Immune System Activation ◽

System Activation

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Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00328.2013 ◽

2014 ◽

Vol 306 (2) ◽

pp. H184-H196 ◽

Cited By ~ 105

Author(s):

Cameron G. McCarthy ◽

Styliani Goulopoulou ◽

Camilla F. Wenceslau ◽

Kathryn Spitler ◽

Takayuki Matsumoto ◽

...

Keyword(s):

Immune System ◽

Innate Immune System ◽

Cell Injury ◽

Receptor Activation ◽

Innate Immune ◽

Immune System Activation ◽

System Activation ◽

Molecular Patterns ◽

Damage Associated Molecular Patterns

Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible changes to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.

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